2. MODULE 3 CHAPTER 2D

3. HYPERTENSION AND CVA

4. The plan Introduction Primary prevention of stroke Management of hypertension during acute stoke Secondary prevention Conclusions

5. Hypertension The leading CVD risk Factor Contributes to 13% global deaths 1 http://www.world-heart-federation.org/press/fact-sheets/cardiovascular-disease-risk-factors/ viewed on May 16, 2013, http://hp2010.nhlbihin.net/joinhin/news/professional/hdrisk.asp 5 An increase in the number and severity of risk factors by middle age can affect a person’s remaining lifetime risk for CVD 2 Prevention and control of CVD risk factors are crucial 2 Hypertension related deaths 13%

6. Hypertension The Indian Scenario > 140 million people have high BP 1 By 2030, it is expected to cross the 214 million 1 Causes more strokes than ACS (34.6% vs 17.9%) In India, Hypertension is responsible for 2 – 57% of all stroke deaths – 24% of all CHD deaths 6 1. http://www.thehindu.com/sci-tech/health/hypertension-major-contributor-to-avoidable-deaths- in-india-who/article4513904.ece, 2. Journal of Human Hypertension (2004) 18, 73–78 Stroke has higher morbidity, mortality and less treatment options and success when compared to CAD So in hypertension management we must aim at preventing strokes

11. The plan Introduction Primary prevention of stroke Management of hypertension during acute stoke Secondary prevention Conclusions

12. Commonly we see.. Pts. with good BP control suddenly develop CVA Pts. with long standing high BP don’t develop any vascular event 12

13. Mean blood pressure The average of several readings of systolic or diastolic pressure (expressed as numbers) Different from mean arterial BP (DBP+1/3 PP) Derived from many clinical visits, Home BP recordings and ABPM 7 to 10 or more BP recordings at different clinical visits are needed to get mean blood pressure Mean BP, thus obtained may be an accurate estimate of usual blood pressure 13

15. BP variability The variation of BP with time Expressed as Standard Deviation (SD) Variation may be for beat to beat (ultra short), over 24hrs (Short term) or visit to visit (long term) Extent of variability is positively related to mean blood pressure 15

16. TO PREVENT STROKE Both mean BP as well as BP variability should be addressed BP variability is assuming lot of importance in the prevention of stroke Control of mean BP without achieving reduction in BP variability may not yield benefits

17. Examples 2 patients,5 visits Patient 1 : 120/130/120/130/120 Mean BP- 620/5 = 124 SD= 5.5 Patient 2: 150/110/130/140/90 Mean BP – 620/5 =124 SD=24.08 The patient 2 has BP variability although both patients have same mean BP 17 SD :Standard Deviation

18. BP variability causes and consequences 18

19. BP Variability Evidences for increased risks 19 Canadian Journal of Cardiology 29 (2013) 557e563 BP VariabilityEffect seen Ohasama prospective study Greater-than-anticipated day-to-day variation in home SBP & DBP Increased 12-year CV and stroke mortality risks 7.8-year follow-up of a representative Finnish population Variability of self measured home BP during 7 consecutive days Independent predictor of subsequent CV events Women’s Health Initiative study of 58,228 postmenopausal women Greater visit-to-visit BP variability Increased risk for both ischemic and hemorrhagic stroke

20. Which drug reduces BP variability 20

21. Visit to visit BPV

22. Stroke risk and coronary risk expressed by docile of within-visit SBP variability Number of patients in each docile of within-visit SD SBP Stroke risk (HR, 95% CI) Coronary risk (HR, 95% CI)

23. ALLHAT TRIAL 23 REDUCTION OF STROKE WAS THE HIGHEST FOR AMLODIPINE MAP BPVMAP BPV MAP: MEAN BP BPV: BP VARIABILITY

24. For primary prevention The most important aspect of primary prevention of stroke is BP control Calcium antagonists especially long acting DHPs are powerful drugs to get BP targets They have additional benefit of reducing BP variability which is emerging as an important risk factor for stroke Even in combination therapy Calcium antagonists should be tried in 2 nd or 3 rd step

25. The plan Introduction Primary prevention of stroke Management of hypertension during acute stoke Secondary prevention Conclusions

27. Early recognition, transport, evaluation and management

28. BP AND ACUTE STROKE The risk of high blood pressure in stroke is U- shaped blood pressure during acute stroke should be neither too low nor too high, either in ischemic or in hemorrhagic stroke However, the treatment of hypertension during acute stroke remains controversial.

29. Auto regulation When the pressure falls cerebral blood flow (CBF) increases due to fall in resistance.

31. In ischemic stroke when there is fall in CBF due to occluded artery, CBF has to be maintained By increase in pressure (BP).

33. But may increase cerebral edema

34. THE NEW DATA In spite of the controversy, the evidence that blood pressure in acute stroke should be treated when it is very high, must be treated in some cases, and can be treated safely, is mounting. The change that has made the greatest difference is the advent of intravenous thrombolytics for acute stroke; Lowering blood pressure in patients with acute stroke eligible for tissue plasminogen activator to achieve blood pressure below 185 mm Hg systolic and below 110 mm Hg diastolic so that tissue plasminogen activator can be given has become standard therapy

35. Avoid BP >180/110

36. ICH

37. Patients who don’t receive tPA At this time, the previous recommendation not to lower the blood pressure during the initial 24 hours of acute ischemic stroke unless the blood pressure is >220/120 mm Hg or there is a concomitant specific medical condition that would benefit from blood pressure lowering remains reasonable.

38. Exceptions Some conditions, such as myocardial ischemia, aortic dissection, and heart failure, may accompany acute ischemic stroke and may be exacerbated by arterial hypertension. When blood pressure management is indicated for a specific medical condition in the setting of concurrent acute cerebral ischemia, an optimal approach has not been determined. At present, blood pressure targets are based on best clinical judgment. A reasonable estimate might be to initially lower the systolic blood pressure by 15% and monitor for neurological deterioration related to the pressure lowering.

39. Ischemic stroke not eligible for thrombolytic therapy

40. Intracranial hemorrhage In both intracerebral hemorrhage (ICH) and subarachnoid hemorrhage (SAH), the approach to blood pressure management must take into account the potential benefits (eg, reducing further bleeding) and risks (eg, reducing cerebral perfusion) of blood pressure lowering.

41. The difficulty Reducing the blood pressure in patients with either ICH or SAH may be beneficial by minimizing further bleeding and continued vascular damage. Patients with an intracranial hemorrhage due to ICH or SAH may have increased intracranial pressure (ICP) due to blood within the cranium. Cerebral perfusion pressure (CPP) equals MAP minus ICP. Thus, increases in MAP may be the only means to maintain CPP above 60 to 70 mmHg, the level necessary to maintain perfusion. Measuring intracranial pressure directly allows blood pressure to be reduced as low as possible while still maintaining the cerebral perfusion pressure above the conservative level of 60 mmHg

42. Guidelines for treatment ICH AND SAH For patients with SBP >200 mmHg or MAP >150 mmHg, consider aggressive reduction of blood pressure with continuous intravenous infusion of medication accompanied by frequent (every five minutes) blood pressure monitoring ●For patients with SBP >180 mmHg or MAP >130 mmHg and evidence or suspicion of elevated ICP, consider monitoring ICP and reducing blood pressure using intermittent or continuous intravenous medication to keep cerebral perfusion pressure in the range of 61 to 80 mmHg ●For patients with SBP >180 mmHg or MAP >130 mmHg and no evidence or suspicion of elevated ICP, consider a modest reduction of blood pressure (eg, target MAP of 110 mmHg or target blood pressure of 160/90 mmHg) using intermittent or continuous intravenous medication, and clinically reexamine the patient every 15 minutes

44. The agents- B Blockers

45. The agents – Sodium Nitroprusside

46. The agents- Calcium Antagonists

47. New therapy

49. The plan Introduction Primary prevention of stroke Management of hypertension during acute stoke Secondary prevention Conclusions

50. Importance of BP control Once the stroke has stabilized, antihypertensive therapy can reduce the rate of recurrent stroke, independent of the baseline blood pressure. Regardless of the regimen, blood pressure reduction should be gradual.

51. APPROACH TO ANTIHYPERTENSIVE THERAPY- Approach Which patients should be treated? When should therapy be initiated? Which antihypertensive drugs should be used? What is the goal blood pressure?

52. Which patients should be treated? With few exceptions, the AHA/ASA stroke prevention guidelines recommend initiation of antihypertensive therapy in all patients who have had an ischemic stroke or TIA However, do not recommend antihypertensive therapy in the following settings: Normotensive patients who have had a stroke or TIA due to a cardio embolic phenomenon (eg, atrial fibrillation) or paradoxical embolus (eg, patent foramen ovale or septal defect). Patients whose initial blood pressure is less than 120/70 mmHg. These patients have an increased risk of recurrent stroke if their blood pressure is further reduced compared with patients who have higher blood pressures.

53. When should therapy be initiated? After the acute management with parenteral anti hypertensive drugs, once pt. is stabilized and is able to take orally, appropriate anti hypertensives should be started according to presence or absence of compelling indications Dosage should be adjusted to achieve target BP without reducing vital organ perfusion

54. Which antihypertensive drugs should be used?- Monotherapy Based upon trial observations, both angiotensin inhibitors (most trials have used ACE inhibitors) and calcium channel blockers are reasonable options for initial antihypertensive therapy in patients who have had a stroke. Thiazide diuretics are also commonly used, but data on monotherapy in patients who have had a stroke are limited. There is some evidence from clinical trials that beta blockers may not reduce stroke risk compared with angiotensin inhibitors, calcium channel blockers, and, in some trials, placebo. Thus, unless there is a compelling indication for their use, beta blockers should not be used for prevention of recurrent stroke

55. The combination of an angiotensin inhibitor plus a long-acting dihydropyridine calcium channel blocker rather than a diuretic is preferred as the combination antihypertensive regimen of choice in the treatment of patients who have had a stroke. This recommendation assumes that the patient can tolerate and does not have a contraindication to the use of either drug class and does not have a specific indication for the use of another class of antihypertensive drugs. Which antihypertensive drugs should be used?- Combination

56. Goal blood pressure The recommendations depend upon whether or not the event was due to a hemodynamically significant stenosis in a large cervicocephalic artery (ie, internal carotid, middle cerebral, vertebral, or basilar artery).

57. In patients with hemodynamically significant large artery disease, it is suggested that cautious blood pressure lowering as tolerated but without a specific blood pressure goal other than a minimum reduction of 10/5 mmHg. However, in such patients whose initial blood pressure is less than 120/70, do not give antihypertensive therapy. Goal blood pressure

58. : In patients without hemodynamically significant large artery stenosis, the following approach is recommended: Lowering the blood pressure a minimum of 10/5 mmHg in nearly all patients Patients whose initial blood pressure is less than 120/70, do not give antihypertensive therapy In patients with underlying hypertension, a goal blood pressure of less than 140/90 mmHg is recommended Lowering the systolic pressure below 130 to 135 mmHg can be tried if it can be achieved without producing significant side effects. Goal blood pressure

59. For patients with recent small vessel (i.e., lacunar) ischemic stroke, lowering the systolic blood pressure below 130 mmHg is recommended provided it can be achieved without side effects : Goal blood pressure

60. The plan Introduction Primary prevention of stroke Management of hypertension during acute stoke Secondary prevention Conclusions

61. Conclusions Case fatality in stroke obeys a U-shaped relationship: blood pressures that are either too low or too high are associated with worse outcomes both in ischemic stroke and in intracerebral hemorrhage. Very high blood pressures should be lowered in acute stroke, and there are some circumstances in which high blood pressure must be treated despite the presence of stroke. To avoid worsening of ischemia by reduction in cerebral blood flow, it is necessary to treat high blood pressure in acute stroke with drugs that can be controlled; this usually means giving drugs by intravenous infusion; However, there is recent evidence that transdermal administration of nitrates, which can be removed if pressure is too low, is a convenient alternative that does not reduce cerebral blood flow in acute stroke.

62. Reduce BP to prevent strokes!

63. END OF MODULE 3 CHAPTER 2D